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. 2022 Feb 25;54(2):194–205. doi: 10.1038/s12276-022-00735-x

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Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Model showing mechanism by which pro-oncogenic trigger may impair the cross-talk among m6A reader IGF2BP3, stabilize m6A-labeled genes and promote the abnormal accumulation of carcinogens (such as Myc, CEBPA, Bcl2, RCC2, etc.), thereby regulating the survival of leukemia cells and leading to AML progression.